Oxidative stress in childhood type 1 diabetes: Results from a study covering the first 20 years of evolution

Abstract

This study aimed to further analyse the potential role of oxidative stress in children and adolescents with type 1 diabetes at clinical onset, during disease progression and when early microvascular complications ( + DC) appeared. Compared with age-matched controls, diabetic patients had greater oxidative damage to lipids, proteins and DNA demonstrated by analysis of plasma and erythrocyte malondialdehyde, carbonyl proteins and leukocyte 8-hydroxy-deoxyguanosine, all of which were significantly raised at onset, decreased during the first 1.5 years of evolution and rose progressively thereafter. Plasma lipid levels were significantly associated with lipid and protein oxidation products. Erythrocyte glutathione and glutathione-peroxidase activity were significantly decreased with the lowest values at onset and in + DC sub-groups. Insulin therapy in the first year improved metabolic and oxidant-antioxidant status and, consequently, hyperglycaemia-derived biomolecular oxidative damage. Diabetes-associated hyperlipidaemia is related to lipid and protein oxidation, thereby supporting the concept of glucotoxicity and lipotoxicity being inter-related. The overall increase in lipid, protein and DNA oxidative damage in diabetic patients with microangiopathy could be pathogenetically relevant in the early development of diabetes-related complications.

• Antioxidant enzymes
• glutathione
• lipid peroxidation
• malondialdehyde
• microvascular complications
• oxidative stress
• protein oxidation
• reactive oxygen species
• type 1 diabetes mellitus

Abbreviations
GSH	=	glutathione
GPx	=	glutathione peroxidase
MDA	=	malondialdehyde
ROS	=	reactive oxygen species
SOD	=	superoxide dismutase
8-OHdG	=	8-hydroxy-2′-deoxyguanosine

Abbreviations
GSH	=	glutathione
GPx	=	glutathione peroxidase
MDA	=	malondialdehyde
ROS	=	reactive oxygen species
SOD	=	superoxide dismutase
8-OHdG	=	8-hydroxy-2′-deoxyguanosine